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Difference between revisions of "Karabatsiakis 2014 Transl Psychiatry"

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{{Publication
{{Publication
|title=Karabatsiakis A, Bock C, Salinas-Manrique J, Kolassa S, Calzia E, Dietrich DE, Kolassa I-T (2014) Mitochondrial respiration in peripheral blood mononuclear cells correlates with depressive subsymptoms and severity of major depression. Translational Psychiatry 4:e397.
|title=Karabatsiakis A, Boeck C, Salinas-Manrique J, Kolassa S, Calzia E, Dietrich DE, Kolassa IT (2014) Mitochondrial respiration in peripheral blood mononuclear cells correlates with depressive subsymptoms and severity of major depression. Transl Psychiatry 4:e397.
|info=[http://www.ncbi.nlm.nih.gov/pubmed/26126180 PMID: 26126180 Open access]
|info=[http://www.ncbi.nlm.nih.gov/pubmed/26126180 PMID: 26126180 Open Access] Β» [[File:O2k-brief.png|36px|link=https://wiki.oroboros.at/images/1/1b/Karabatsiakis_2014_Transl_Psychiatry_O2k-brief.pdf |O2k-brief]]
|authors=Karabatsiakis A, Bock C, Salinas-Manrique J, Kolassa S, Calzia E, Dietrich DE, Kolassa IT
|authors=Karabatsiakis Alexander, Boeck Christina, Salinas-Manrique J, Kolassa S, Calzia Enrico, Dietrich DE, Kolassa Iris
|year=2014
|year=2014
|journal=Translational Psychiatry
|journal=Transl Psychiatry
|abstract=Mitochondrial dysfunction might have a central role in the pathophysiology of depression. Phenotypically, depression is characterized by lack of energy, concentration problems and fatigue. These symptoms might be partially explained by reduced availability of adenosine triphosphate (ATP) as a consequence of impaired mitochondrial functioning. This study investigated mitochondrial respiration in peripheral blood mononuclear cells (PBMCs), an established model to investigate the pathophysiology of depression. Mitochondrial respiration was assessed in intact PBMCs in 22 individuals with a diagnosis of major depression (MD) compared with 22 healthy age-matched controls using high-resolution respirometry. Individuals with MD showed significantly impaired mitochondrial functioning: routine and uncoupled respiration as well as spare respiratory capacity, coupling efficiency and ATP turnover-related respiration were significantly lower in the MD compared with the control group. Furthermore, mitochondrial respiration was significantly negatively correlated with the severity of depressive symptoms, in particular, with loss of energy, difficulties concentrating and fatigue. The results suggest that mitochondrial dysfunction contributes to the biomolecular pathophysiology of depressive symptoms. The decreased immune capability observed in MD leading to a higher risk of comorbidities could be attributable to impaired energy supply due to mitochondrial dysfunction. Thus mitochondrial respiration in PBMCs and its functional consequences might be an interesting target for new therapeutical approaches in the treatment of MD and immune-related comorbidities
|abstract=Mitochondrial dysfunction might have a central role in the pathophysiology of depression. Phenotypically, depression is characterized by lack of energy, concentration problems and fatigue. These symptoms might be partially explained by reduced availability of adenosine triphosphate (ATP) as a consequence of impaired mitochondrial functioning. This study investigated mitochondrial respiration in peripheral blood mononuclear cells (PBMCs), an established model to investigate the pathophysiology of depression. Mitochondrial respiration was assessed in intact PBMCs in 22 individuals with a diagnosis of major depression (MD) compared with 22 healthy age-matched controls using high-resolution respirometry. Individuals with MD showed significantly impaired mitochondrial functioning: routine and uncoupled respiration as well as spare respiratory capacity, coupling efficiency and ATP turnover-related respiration were significantly lower in the MD compared with the control group. Furthermore, mitochondrial respiration was significantly negatively correlated with the severity of depressive symptoms, in particular, with loss of energy, difficulties concentrating and fatigue. The results suggest that mitochondrial dysfunction contributes to the biomolecular pathophysiology of depressive symptoms. The decreased immune capability observed in MD leading to a higher risk of comorbidities could be attributable to impaired energy supply due to mitochondrial dysfunction. Thus mitochondrial respiration in PBMCs and its functional consequences might be an interesting target for new therapeutical approaches in the treatment of MD and immune-related comorbidities
|keywords=PBMC
|mipnetlab=DE Ulm Karabatsiakis A, DE Ulm Radermacher P
|mipnetlab=DE Ulm Karabatsiakis A, DE Ulm Radermacher P
}}
}}
{{Labeling
{{Labeling
|area=Respiration, mt-Medicine, Patients
|area=Respiration, Instruments;methods, mt-Medicine, Patients
|diseases=Neurodegenerative
|injuries=Cryopreservation
|organism=Human
|organism=Human
|tissues=Blood cells
|tissues=Blood cells
|preparations=Intact cells
|preparations=Intact cells
|injuries=Cryopreservation
|couplingstates=LEAK, ROUTINE, ET
|diseases=Neurodegenerative, Other
|pathways=ROX
|couplingstates=LEAK, ROUTINE, ETS
|substratestates=ROX
|instruments=Oxygraph-2k
|instruments=Oxygraph-2k
|additional=MitoFit news
|additional=BMI, Comorbidity, MitoEAGLE blood cells data, PBMC, O2k-brief
}}
}}
[[File:O2k-brief.png|36px|left]]
== O2k-brief ==
::::Β» [[O2k-brief |List of O2k-Publications presented as O2k-brief]]
[[Image:Logo MitoFit.jpg|right|120px|link=http://www.mitofit.org/index.php/MitoFit|MitoFit]]
== MitoFit news 2015#2 ==
== MitoFit news 2015#2 ==
* 2015-05-08: Depressed cellular energetics correlates with depressive states of mind: high-resolution respirometry in blood cells (PBMCs). Β»[[MitoFit news]]
* 2015-05-08: Depressed cellular energetics correlates with depressive states of mind: high-resolution respirometry in blood cells (PBMCs). Β»[[K-Regio_MitoFit#2015 |MitoFit news]]
* [[Microwell_respirometry#Respirometry_with_cryopreserved_blood_cells |Respirometry with cryopreserved blood cells]]
* [[Microwell_respirometry#Respirometry_with_cryopreserved_blood_cells |Respirometry with cryopreserved blood cells]]

Revision as of 08:25, 10 August 2020

Publications in the MiPMap
Karabatsiakis A, Boeck C, Salinas-Manrique J, Kolassa S, Calzia E, Dietrich DE, Kolassa IT (2014) Mitochondrial respiration in peripheral blood mononuclear cells correlates with depressive subsymptoms and severity of major depression. Transl Psychiatry 4:e397.

Β» PMID: 26126180 Open Access Β» O2k-brief

Karabatsiakis Alexander, Boeck Christina, Salinas-Manrique J, Kolassa S, Calzia Enrico, Dietrich DE, Kolassa Iris (2014) Transl Psychiatry

Abstract: Mitochondrial dysfunction might have a central role in the pathophysiology of depression. Phenotypically, depression is characterized by lack of energy, concentration problems and fatigue. These symptoms might be partially explained by reduced availability of adenosine triphosphate (ATP) as a consequence of impaired mitochondrial functioning. This study investigated mitochondrial respiration in peripheral blood mononuclear cells (PBMCs), an established model to investigate the pathophysiology of depression. Mitochondrial respiration was assessed in intact PBMCs in 22 individuals with a diagnosis of major depression (MD) compared with 22 healthy age-matched controls using high-resolution respirometry. Individuals with MD showed significantly impaired mitochondrial functioning: routine and uncoupled respiration as well as spare respiratory capacity, coupling efficiency and ATP turnover-related respiration were significantly lower in the MD compared with the control group. Furthermore, mitochondrial respiration was significantly negatively correlated with the severity of depressive symptoms, in particular, with loss of energy, difficulties concentrating and fatigue. The results suggest that mitochondrial dysfunction contributes to the biomolecular pathophysiology of depressive symptoms. The decreased immune capability observed in MD leading to a higher risk of comorbidities could be attributable to impaired energy supply due to mitochondrial dysfunction. Thus mitochondrial respiration in PBMCs and its functional consequences might be an interesting target for new therapeutical approaches in the treatment of MD and immune-related comorbidities β€’ Keywords: PBMC

β€’ O2k-Network Lab: DE Ulm Karabatsiakis A, DE Ulm Radermacher P


Labels: MiParea: Respiration, Instruments;methods, mt-Medicine, Patients  Pathology: Neurodegenerative  Stress:Cryopreservation  Organism: Human  Tissue;cell: Blood cells  Preparation: Intact cells 


Coupling state: LEAK, ROUTINE, ET  Pathway: ROX  HRR: Oxygraph-2k 

BMI, Comorbidity, MitoEAGLE blood cells data, PBMC, O2k-brief 

O2k-brief.png

O2k-brief

Β» List of O2k-Publications presented as O2k-brief
MitoFit

MitoFit news 2015#2